Stressed mammalian cells up-regulate heme oxygenase 1 (HO-1), which catabolizes heme to biliverdin, carbon monoxide, and free iron. Results provide genetic evidence that up-regulation of HO-1 serves as an adaptive mechanism to protect cells from oxidative damage during stress (1). When cells are injured they release their contents, resulting in a local accumulation of free heme proteins and heme. HO-1 plays a crucial role in the inflammatory process during wound healing (2). TNFalpha accelerates inflammatory responses by down-regulating HO-1 expression in human monocytes. TNF antagonists may block this TNF-dependent suppression of HO-1 expression, resulting in an amelioration of inflammation (3).